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<p>Enfortumab vedotin (EV) is a&#xa0;targeted antibody-drug conjugate (ADC) directed against NECTIN4 and approved for treatment of metastatic urothelial carcinoma (mUC) after failure of platinum-based chemotherapy and immune checkpoint inhibitors. However, not all patients benefit equally from EV, highlighting the need for a&#xa0;predictive biomarker. In this multicenter study, 108 EV-treated mUC patients were analyzed for genomic <i>NECTIN4</i> amplifications using fluorescence in situ hybridization (FISH). Approximately one-quarter of tumors showed <i>NECTIN4</i> amplification, which was strongly associated with increased membranous protein expression and an objective response rate of 96%. Amplified tumors also had significantly prolonged overall survival. In a&#xa0;control cohort without EV, <i>NECTIN4</i> amplification had no prognostic impact. These findings identify <i>NECTIN4</i> amplification as a&#xa0;stable, predictive biomarker that may guide treatment decisions in mUC. Data from TCGA further suggest a&#xa0;cross-entity relevance of <i>NECTIN4</i> amplification, supporting future clinical exploration of EV in other solid tumors.</p>

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NECTIN4-Amplifikation als prädiktiver Biomarker für das Ansprechen auf Enfortumab-Vedotin

  • 期刊论文

  • 发表日期：

    2025年11月14日

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  • Markus Eckstein

摘要

Enfortumab vedotin (EV) is a targeted antibody-drug conjugate (ADC) directed against NECTIN4 and approved for treatment of metastatic urothelial carcinoma (mUC) after failure of platinum-based chemotherapy and immune checkpoint inhibitors. However, not all patients benefit equally from EV, highlighting the need for a predictive biomarker. In this multicenter study, 108 EV-treated mUC patients were analyzed for genomic NECTIN4 amplifications using fluorescence in situ hybridization (FISH). Approximately one-quarter of tumors showed NECTIN4 amplification, which was strongly associated with increased membranous protein expression and an objective response rate of 96%. Amplified tumors also had significantly prolonged overall survival. In a control cohort without EV, NECTIN4 amplification had no prognostic impact. These findings identify NECTIN4 amplification as a stable, predictive biomarker that may guide treatment decisions in mUC. Data from TCGA further suggest a cross-entity relevance of NECTIN4 amplification, supporting future clinical exploration of EV in other solid tumors.